# Ovarian aging, cardiovascular risk and inflammation: insights from the OVA study

## TL;DR

This study explores whether inflammation connects ovarian aging and cardiovascular risk in women but finds limited evidence for this link.

## Contribution

The study provides new insights into the lack of consistent associations between inflammation, ovarian aging, and cardiovascular risk in premenopausal women.

## Key findings

- No significant associations were found between inflammatory markers, metabolic syndrome, and ovarian aging measures in cross-sectional analysis.
- Higher levels of IL-6 and TNF-α were associated with the Framingham Risk Score in longitudinal analysis.
- The findings suggest that inflammation may not be a central mechanism linking ovarian aging to cardiovascular risk.

## Abstract

Cardiovascular disease is the leading cause of death among women and is associated with both metabolic syndrome and ovarian aging. Chronic inflammation has been proposed as a potential common underlying mechanism linking these conditions. This study aimed to examine the associations between inflammatory markers (interleukin-6, tumor necrosis factor-alpha, high-sensitivity C-reactive protein) and metabolic syndrome, with markers of ovarian aging and cardiovascular risk.

In the cross-sectional analysis of 829 women aged 25–45, no significant associations were found between inflammatory markers, metabolic syndrome, and ovarian aging measures (anti-Müllerian hormone [AMH] and antral follicle count [AFC]), except for a modest association between metabolic syndrome and AMH (mean difference 0.085; 95% CI: 0.035 to 0.134). Similarly, inflammatory markers and metabolic syndrome were not significantly associated with the Framingham Risk Score. In the longitudinal analysis of 307 participants, changes in AMH and AFC were not associated with inflammatory markers or metabolic syndrome. However, higher levels of IL-6 and TNF-α were associated with the Framingham Risk Score, whereas hsCRP and metabolic syndrome were not.

These findings do not support the hypothesis that inflammation is a central mechanism linking ovarian aging to cardiovascular risk. The absence of consistent associations across analyses suggests that alternative pathways may underlie this relationship. Further research incorporating a broader range of biomarkers is warranted to elucidate the complex interactions between reproductive aging and cardiovascular health in women.

The online version contains supplementary material available at 10.1186/s13048-025-01754-8.